Abstract

The infection of tomato fruit by the postharvest pathogen Colletotrichum gloeosporioides did not proceed until the onset of ripening in response to ethylene. Compared with fruit from wild-type plants, infection progressed more slowly in transgenic fruit in which ethylene biosynthesis and ripening had been inhibited by an ACC oxidase (ACO) antisense transgene. In contrast, transgenic fruit deficient in polygalacturonase developed lesions at the same rate as the wild-type fruit. Ethylene biosynthesis increased rapidly in response to infection of ripe wild-type and ACO antisense fruit but was 25 times greater in the former. Fruit from the ripening mutant ripening inhibitor (rin), which are normally very resistant to infection, became infected quickly when incubated in the presence of ethylene, whereas fruit incubated in the absence of ethylene remained healthy. The ACO 1 mRNA accumulated to detectable levels within 24 h of inoculation of unripe wild-type fruit, prior to the development of visible symptoms, whereas there was no detectable expression in the inoculated ACO antisense fruit. ACO transcripts accumulated to maximum levels during the early stages of infection of ripe fruit, correlating with maximum ethylene biosynthesis. Northern analysis using gene-specific probes for each of the three ACO genes indicated that ACO 1 was the main gene expressed in response to infection and that there was no detectable expression of ACO 2 and 3.

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Article

Additional Information:

The definitive version is available at http://www3.interscience.wiley.com The original PDF of the article can be found at Plant Pathology website : http://www3.interscience.wiley.com/journal/119112395/abstract